據(jù)《美國心臟病學會雜志》最近出版的一文章稱,，荷蘭的科學家研究發(fā)現(xiàn)，脂蛋白水平和纖維蛋白原的水平升高與斑塊進展和心血管事件的危險升高有相關性,。

　　荷蘭Medish  Psectrum  Twente的研究人員為了評估Lp(a)和纖維蛋白原是否可預測不良心血管事件風險,，入選了60例受試，分析其非狹窄冠狀動脈的斑塊進展情況,。

　　結果發(fā)現(xiàn),，Lp(a)和纖維蛋白原的水平與斑塊-基質(zhì)面積呈正相關，有斑塊進展的患者Lp(a)水平明顯高于沒有斑塊進展者,，兩組的纖維蛋白原的水平也有類似結果,，但多變量分析表明，只有Lp(a)的對數(shù)水平與斑塊進展獨立相關,。

　　在18個月的隨訪研究中發(fā)現(xiàn),，發(fā)生心血管事件患者的Lp(a)水平和纖維蛋白原水平明顯高于與沒發(fā)生事件的患者,，其纖維蛋白原水平也高于沒有發(fā)生不良心血管事件的患者。

　　研究人員稱,，該研究提示,，Lp(a)  和纖維蛋白原水平與斑塊-基質(zhì)面積的年改變呈正相關，而Lp(a)水平大幅提高可預測心血管危險,。

英文原文：

　　　Lp(a) and fibrinogen linked to plaque progression

Dutch scientists have found elevated lipoprotein (Lp)(a) and fibrinogen levels are associated with plaque progression and a higher risk of cardiovascular (CV) events.
March Hartmann (Medish Psectrum Twente, Enschede) and colleagues analyzed plaque progression in the non-stenotic coronary arteries of 60 individuals to test whether Lp(a) and fibrinogen levels could predict the onset of adverse CV events.

Both Lp(a) and fibrinogen levels were positively correlated with plaque-plus-media area. Patients with evidence of plaque progression had significantly higher levels of Lp(a) than those without, at 30 mg/dl versus 14 mg/dl, as well as significantly higher levels of fibrinogen, at 295 mg/dl versus 240 mg/dl.

However, after multivariate analysis, only log levels of Lp(a) were independently associated with plaque progression.

The team found that levels of Lp(a) were significantly higher in the 19 patients who experienced adverse CV events within the 18-months of follow-up than in those who remained free of CV events, at 44 and 16 mg/dl, respectively.

Fibrinogen levels were also higher in these 19 patients who experienced CV events than those who experienced no adverse CV events, at 342 mg/dl versus 248 mg/dl.

Unlike plaque progression, multivariate analysis demonstrated that both log levels of Lp(a) and fibrinogen were independently associated with adverse CV events.

"We found a positive correlation between Lp(a) and fibrinogen levels versus annual changes in plaque-plus-media area," write March Hartmann et al in the Journal of the American College of Cardiology.

"The data suggest in particular a considerable incremental value of Lp(a) in predicting cardiovascular risk."

Lp(a) may be involved in atherosclerosis, they conclude, due to its accumulation in the vessel wall, ability to promote foam cell cholesterol accumulation and smooth muscle cell proliferation, and finally through its inactivation of growth factor-beta transformation.